Colour Vision in Patients Suspected of Intoxication

Abstract

About 700 patients suspected of intoxication or being on treatment were examined by means of elaborate colour vision testing. Optic nerve pathology was found with amiodarone, practolol, clioquinol, thallium, alcohol/tobacco abuse and steroids/cytostatics. Retinal pathology was seen in patients on medication with digitoxin and chloroquin.

Both retinal and optic nerve dysfunction were found in patients treated with salazosulfapyridine, tuberculostatics and analgetics. ‘Effects of intoxications on colour vision’ is a special theme of the present symposium. It is not easy to establish an intoxication. It is often not possible to differentiate effects of drug therapy from complications of the underlying disease. In many patients more than one drug are prescribed at the same time: is the intoxication the result of a single drug or is it the result of interaction of two or even more drugs or of their metabolites? Even the diet of the patient, the condition of the intestinal flora (vitamin synthesis) and the consumption of alcohol or tobacco may play an important role.

For this symposium I investigated the files of about 700 patients suspected of intoxication or being on treatment. The purpose was to select patients in whom colour vision examination strongly suggested involvement of the retina or of the optic nerve. Colour vision examination was made under standardized conditions: six Philips fluorescent tubes colour 57, colour rendering index 96, providing 1750 lux at the level of the test table. I made a choice out of 8° tests (AOIH-R-R,TMC, Ishihara, F2-plate, SPP-part II), 2° tests (FM 100 Hue, New Color Test, Desaturated D-15) and an anomaloscope (Nagel II, Neitz OT or Pickford-Nicolson).

In 1 of 13 patients on amiodarone therapy colour vision indicated bilateral optic nerve pathology; this finding does not mean, however, that amiodarone is the real cause of optic nerve dysfunction. The same holds true for practolol (3 of 14 patients had bilateral optic nerve pathology) although we know that this drug was a very dangerous one (retroperitoneal fibrosis and lacrimal gland atrophy). The UO-test was abnormal in 9 of 11 cases examined.

Subacute myelo-optic neuropathy is due to iodchlor-hydroxyquinoline (Clioquinol; Matsuo et al., 1971). In one of the two cases examined I also noticed a keratopathy of the verticillata type (Bron et al., 1972). In thallium poisoning 10 of the 12 eyes examined evidenced a type II acquired red-green defect (Girot and Braum, 1929; Pinckers, 1975).

Synthetical antimalarial agents are selectively accumulated in the choroid and the retinal pigment epithelium (Lawwill et al., 1968). In untreated rheumatoid arthritis patients and in patients with chloroquine or hydroxychloroquine medication without funduscopic retinal abnormalities the ratio normal colour vision to sensitivity decrease is about the same (Table 2). In chloroquine treated subjects with a bull’s eye maculopathy colour vision often is disturbed, the diminished red sensitivity being a sign of receptor misalignment (Table 1).

The type II acquired red-green defect in patients treated with tuberculostatics is not surprising (Vérin et al., 1971; Ourou et al., 1972; Douche, 1974; Trusiewicz, 1975; Derka, 1975). The nine eyes with diminished red sensitivity (Table 1) indicating retinal involvement all had funduscopic retinal alterations. I have no idea whether this retinal pathology is related to the underlying disease or to the medication.

In salazosuljapyridine-treated subjects I found signs of optic nerve pathology and also signs of retinal involvement, the latter again showing funduscopic retinal alterations (Table 1). The clinical aspect of the fundus changes, e.g., retinal drusen, rpe alterations and choroidal atrophy, are probably related to neither the underlying chronic bowel disease nor the medication.

About 1/3 of the patients on treatment with analgetics had more than one drug at the same time (Table 3). In the subgroup presenting with a type II acquired red-green defect there is a predominance of ibuprofen therapy (Collum and Bowen, 1971). In the two patients who had only ibuprofen as medication withdrawal resulted in complete recovery of colour vision (Pinckers, 1975).

Patients receiving oral corticosteroid therapy and/or cytostatics had normal colour vision or a nonspecific sensitivity decrease or a type II acquired red-green defect. Two of three eyes with optic nerve pathology had a corticosteroid-induced glaucoma.